Slideshow
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Figure 1. A multicolored plaque consisting of red, purple, and black hues 1.5 cm in diameter is located on the midoccipital scalp.
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Figure 2. Nontender dome-shaped soft nodule with telangiectasia.
A 38-year-old man is referred for evaluation of 1.5 cm tender, nonhealing lesion located on the back of his head. The lesion was misdiagnosed in the emergency department (ED) as an abscess; when lanced, the ED clinicians discovered a solid mass. Mupirocin 2% topical ointment and cephalexin 500 mg twice daily were prescribed and an emergent referral was placed. The patient is seen 2 days later in the dermatology office.
The patient states that he first noticed the lesion 3 months ago and it has been gradually increasing in size. He notes that the lesion has become painful, making it hard for him to sleep at night. On physical examination, a multicolored plaque consisting of red, purple, and black hues 1.5 cm in diameter is located on the midoccipital scalp. A second, nontender, dome-shaped soft nodule with telangiectasia is seen on the patient’s right upper arm. The patient states that the lesion has been present for almost 2 years. Although smaller than the scalp lesion, this lesion is rapidly growing in both width and height. The clinician orders a biopsy of both lesions.
The patient’s medical history includes diabetes mellitus, hypertension, and presence of a lazy eye. He has no known family history of cancer and drinks 1 alcoholic beverage per day. Smoking history is positive for 1 pack a day and he is currently taking lisinopril 10 mg and metformin 500 mg daily.
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Discussion
Biopsy results of the lesion on the occipital scalp are positive for a nodular melanoma with Breslow thickness of 2.8 mm involving the deep margins. Clark classification is level IV, indicating invasion of cancerous cells into the reticular dermis layer of the skin — the lesion is classified as T3B. The biopsy results from the right upper arm are positive for a spindle cell pleomorphic lipoma, which is benign and can be managed with continued clinical follow-up.
Melanoma is the most serious form of skin cancer accounting for 5.2% of all new cancer cases and 1.6% of all cancer deaths; it is the fifth most common cancer in both men and women.1 Risk factors for developing melanoma include a family history of skin cancer, living in sunny climates or at high altitudes, fair skin, repeated exposure to radiographs, immunosuppression, presence of atypical melanocytic nevi, and scarring from disease, injury, or burns.2 The major survival determinant for people with melanoma depends on the stage of the disease at the time of diagnosis; therefore, it is crucial to educate patients on the importance of performing regular skin checks and to schedule visits to skilled dermatologists for examination of suspicious lesions.
The 4 major subtypes of invasive cutaneous melanoma include superficial spreading, nodular, lentigo maligna, and acral lentiginous. Approximately 70% to 80% of all melanomas are superficial spreading and commonly arise in a pre-existing nevus.1 Superficial melanomas tend to be larger than 6 mm and spread in a horizontal or “radial” growth phase. Nodular melanomas make up about 15% to 30% of all melanomas.3 The trunk, head, and neck are regions of the body most commonly affected by nodular melanomas and they are considered to be in a “vertical” growth phase with strong metastatic potential.4 Nodular melanomas result in thicker tumors at the time of diagnosis and grow quickly over the period of several weeks to months.5 Lentigo maligna melanoma is commonly seen in chronically sun-damaged regions of the skin and often begin as a tan or dark macule and account for 10% to 15% of all melanomas.2 Acral lentiginous melanomas account for less than 5% of all melanomas and are most common among darker pigmented individuals. These cancers evolve over a period of years and are more often seen on the palms, soles, and around the nails.6
Visual analysis of melanoma takes into account the widely adapted ABCDE checklist: asymmetry, border irregularity, color variegation, diameter >6 mm, and evolution.5 Nodular melanomas and those with little to no pigmentation have the added EFG criteria: elevation, firm on palpation, and continuous growth for 1 month or longer.7 The ugly duckling sign is another useful technique to help determine a pigmented lesion that is obviously different among multiple nevi. These diagnostic criteria are important factors in the evaluation of melanoma among intrapatient comparative analyses.8
The initial diagnosis of melanoma is made by several means, some of which include dermoscopy, reflectance confocal microscopy, and multispectral imaging-based systems.9 Characteristic of melanoma under dermatoscopic examination may consist of atypical network of pigment, irregular brown-black globules, and an atypical vascular pattern. Reflectance confocal microscopy (RCM) allows for the in-vivo identification of cells using a low-power laser that emits infrared light, creating a clear 3-dimensional image of the suspicious lesion.10
Definitive diagnosis of melanoma is made either by excisional/complete or incisional biopsy. Genetic testing is an important player in both initial diagnosis and preventing future progression of melanoma. Expression of the LINC and PRAME genes is highly correlated to melanoma development; patients with overexpression of these genes tend to show mutations in BRAF, NRAS, and TERT genes, which are directly involved in melanoma progression.11
Sogol Pahlevan, PA-S, is a physician associate student. Srikanth Vangapandu, MD (Ukraine), MPH, MSPAS, PA-C, currently works as a dermatology PA at Dermatologists of Central States in Ohio.
References
1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2019. CA Cancer J Clin. 2019;69(1):7-34. doi:10.3322/caac.21551.
2. Habif TP, Dinulos JGH, Chapman MS, Zug KA, eds. Skin Disease, 4th ed. Elsevier; 2018.
3. Elder DE, Bastian BC, Cree IA, Massi D, Scolyer RA. The 2018 World Health Organization classification of cutaneous, mucosal, and uveal melanoma: detailed analysis of 9 distinct subtypes defined by their evolutionary pathway. Arch Pathol Lab Med. 2020;144(4):500-522. doi:10.5858/arpa.2019-0561-RA
4. Hassel JC, Enk AH. Melanoma. In: Kang S, Amagai M, Bruckner AL, et al, eds. Fitzpatrick’s Dermatology, 9th ed. McGraw-Hill Education; 2019:1980-1985.
5. American Academy of Dermatology Ad Hoc Task Force for the ABCDEs of Melanoma, Tsao H, Olazagasti JM, et al. Early detection of melanoma: reviewing the ABCDEs. J Am Acad Dermatol. 2015;72(4):717-723. doi:10.1016/j.jaad.2015.01.025
6. Swetter SM, Elston DM. Cutaneous melanoma clinical presentation: history, physical examination, complications. Medscape. Updated April 29, 2019. Accessed July 28, 2021. https://emedicine.medscape.com/article/1100753-clinical
7. Dinnes J, Deeks JJ, Chuchu N, et al. Dermoscopy, with and without visual inspection, for diagnosing melanoma in adults. Cochrane Database Syst Rev. 2018;12(12):CD011902. doi:10.1002/14651858.CD011902.pub2.
8. Elmore JG, Barnhill RL, Elder DE, et al. Pathologists’ diagnosis of invasive melanoma and melanocytic proliferations: observer accuracy and reproducibility study. BMJ. 2017;357:j2813. doi:10.1136/bmj.j2813 2017; 357.
9. Cancer Genome Atlas Network. Genomic classification of cutaneous melanoma. Cell. 2015;161(7):1681-1696. doi:10.1016/j.cell.2015.05.04
10. Shain AH, Yeh I, Kovalyshyn I, et al. The genetic evolution of melanoma from precursor lesions. N Engl J Med. 2015;373(20):1926-1936. doi:10.1056/NEJMoa1502583
11. Bolognia JL, Schaffer JV, Duncan KO, Ko CJ, eds. Dermatology Essentials. 1st ed. Elsevier; 2014.
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